JOURNAL OF THE LOUISIANA STATE MEDICAL SOCIETY
TREATMENT
CONCLUSION
Sublingual or oral administration of nitroglycerin or isosorbide dinitrate can treat coronary vasospastic attacks. The failure of nitroglycerin containing medications to relieve coronary spasm in some patients may be explained by: 1) coronary spasm related decreased blood flow to the vasa vasorum that prevents drug delivery to the stenotic segment and 2) systemic vasodilatation by nitroglycerine that can induce a sympathetic reflex which works against the intended therapeutic effect. 18 For these reasons, administration of nitroglycerin via the intracoronary route is the ideal treatment strategy for severe and /or refractory coronary arterial spasm during coronary catheterization. This allows higher concentrations of nitroglycerine and its direct smooth muscle relaxing effects at the site of the coronary spasm. 8 Resistance to intracoronary nitroglycerin does exist and may be the result of the inability of ischemic myocardium to metabolize nitrates. In such settings, intracoronary calcium channel blockers should be considered. Calcium channel blockers have been shown to be superior to nitroglycerin in the treatment of spasms and the prophylaxis against future attacks. The RhoA/ROCK pathway is one of the mechanisms that play a central role in coronary vasospasm. 19 In this pathway, Rho- kinase acts to increase vascular smooth muscle contraction by reducing myosin phosphatase activity and displaying a “calcium sensitization” effect. Fasudil is a potent Rho-kinase inhibitor that has shown to be effective in treating patients with vasospastic angina. Masumoto et al. demonstrated that Fasudil was effective in reducing acetylcholine-induced coronary spasm but had no effect on non-spastic segments. This suggests that Fasudil may be a more selective alternative to calcium channel blockers in the treatment of coronary arterial spasm. 20 L-Arginine may also be an effective treatment for coronary vasospasm. L-arginine is the precursor of endothelium released NO, which is the most important vasodilator derived from the endothelium. Egashira et al. found that L-arginine is an effective vasodilator of coronary microvasculature in patients with microvascular angina. Nevertheless, this study failed to demonstrate any vasodilating role of L-arginine in large epicardial vessels. 21 Therefore, further studies are necessary to prove the effectiveness of oral L-arginine in coronary arterial spasm. This case of life-threatening multivessel coronary arterial spasm appears to have been caused by pregnancy related endocrine changes and/or an aberrant response of the immune system that may have been triggered by fetal antigen. To the authors’ knowledge, there are very few peripartum cases reported in the literature. There appears to be an increased incidence of peripartum coronary arterial spasm in multigravida patients, and these patients typically have an excellent response to intracoronary nitroglycerin and verapamil. All of this deserves further investigation.
Myocardial infarction is rare in the postpartum period and coronary spasm is one of its least probable causes, making its diagnosis difficult and potentially easily missed. Physicians should consider this condition in their differential diagnosis in cases of postpartum myocardial infarction, and in patients with myocardial ischemiaandnormal coronaryangiograms. Although there are many treatment options, nitrates are still considered the best treatment measure. Intracoronary administration of nitroglycerin has been shown to be effective in refractory cases and can be administered either in isolation or in combination with calcium channel blockers to prevent recurrent spasm.
REFERENCES
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104 J La State Med Soc VOL 169 JULY/AUGUST 2017
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